IL-17A is originally identified as a proinflammatory cytokine that induces neutrophils. Although IL-17A production by CD4+ Th17 T cells is well documented, it is not clear whether IL-17A is produced and participates in the innate immune response against infections. In the present report, we demonstrate that IL-17A is expressed in the liver of mice infected with Listeria monocytogenes from an early stage of infection. IL-17A is important in protective immunity at an early stage of listerial infection in the liver because IL-17A-deficient mice showed aggravation of the protective response. The major IL-17A-producing cells at the early stage were TCR γδ T cells expressing TCR Vγ4 or Vγ6. Interestingly, TCR γδ T cells expressing both IFN-γ and IL-17A were hardly detected, indicating that the IL-17A-producing TCR γδ T cells are distinct from IFN-γ-producing γδ T cells, similar to the distinction between Th17 and Th1 in CD4+ T cells. All the results suggest that IL-17A is a newly discovered effector molecule produced by TCR γδ T cells, which is important in innate immunity in the liver.

SummaryMurine cd T cells participate in the innate immune response against infection by an intracellular pathogen Listeria monocytogenes. Vd1 + cd T cells coexpressing Vc6 are a major cd T-cell subpopulation induced at an early stage of L. monocytogenes infection in the livers of infected mice. To investigate the protective role of the Vc6/ /Vd1 + cd T cells against L. mono-) mice were analysed because these mice selectively lacked a Vc6/ /Vd1 + cd T-cell subpopulation in the L. monocytogenes-infected liver. The Vd1 )/) mice showed increased bacterial burden in the liver and spleen, and decreased survival rate at an early stage of L. monocytogenes infection when compared to wild-type mice. Histological examination showed abscess-like lesions and unorganized distribution of macrophages in the liver of the Vd1 )/) mice but not in the wild-type mice after L. monocytogenes infection. The Vc6/ /Vd1 + cd T cells produced interferon-c and interleukin-17A. All the results suggest that murine Vc6/ /Vd1 + cd T cells control the innate protective response against L. monocytogenes infection through production of the proinflammatory cytokines interferon-c and interleukin-17A in the infected liver.

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